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Cerebrospinal fluid Alzheimer's biomarker profiles in CNS infections.

Artikel i vetenskaplig tidskrift
Författare Jan Jessen Krut
Henrik Zetterberg
Kaj Blennow
Paola Cinque
Lars Hagberg
Richard W Price
Marie Studahl
Magnus Gisslén
Publicerad i Journal of neurology
Volym 230
Sidor 620-626
ISSN 1432-1459
Publiceringsår 2013
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 620-626
Språk en
Länkar dx.doi.org/10.1007/s00415-012-6688-...
Ämnesord Bacterial infections, Central nervous system, Herpes encephalitis, HIV-associated dementia (MesH term AIDS dementia complex), Amyloid Tau protein
Ämneskategorier Infektionsmedicin

Sammanfattning

The cerebrospinal fluid (CSF) biomarker profile in Alzheimer's disease (AD) is characterized by decreased beta amyloid (Aβ(1-42)), increased total and hyperphosphorylated tau (t-tau and p-tau, respectively), which is a useful diagnostic tool and gives insight in the pathogenesis of AD. It is of importance to study how these biomarkers react in other CNS diseases; therefore, we decided to analyse amyloid and tau biomarkers in different CNS infections. We also included analysis of soluble amyloid precursor proteins (sAPPα and -β). CSF Aβ(1-42), sAPPα and -β, t-tau and p-tau were analysed in bacterial meningitis (n = 12), Lyme neuroborreliosis (n = 13), herpes simplex virus type 1 (HSV-1) encephalitis (n = 10), HIV-associated dementia (HAD) (n = 21), AD (n = 21) and healthy controls (n = 42). Concurrent with AD, Aβ(1-42) was decreased in all groups except neuroborreliosis compared to controls. HSV-1 encephalitis, bacterial meningitis and HAD showed lower concentrations of sAPPα and -β compared to AD. T-tau was increased in AD and HSV-1 encephalitis compared to all other groups. P-tau was higher in AD and HSV-1 encephalitis compared to bacterial meningitis, HAD and control. Decreased CSF Aβ(1-42), sAPPα and -β in various CNS infections imply an effect of neuroinflammation on amyloid metabolism which is similar in regard to AD concerning Aβ(1-42), but differs concerning sAPPα and -β. These results clearly indicate different pathologic pathways in AD and infectious CNS disease and may provide help in the differential biomarker diagnostics. Increased p-tau in HSV-1 encephalitis probably reflect acute neuronal damage and necrosis.

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